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Serotonin Transporter Deficiency Drives Estrogen-dependent Obesity And Glucose Intolerance


Oct 30, 2015
This 2017 study here is making me scratch my head.
Serotonin transporter deficiency drives estrogen-dependent obesity and glucose intolerance

So these people genetically deleted the serotonin transporter in a group of mice, and pharmacologically antagonized it with an SSRI in another group of mice, and had both on normal diets.

They found that "SERT−/− mice display abnormal fat accumulation in both white and brown adipose tissues, glucose intolerance and insulin resistance," and in the SSRI-group similarly, "treatment of wild type mice with paroxetine... [caused] abnormal fat accumulation, and glucose intolerance." So, low/nonexistent SERT-function makes you fat and insulin resistant, so far so good.

But in both these groups they also found the mice "exhibiting suppressed aromatase (Cyp19a1) expression and [having] reduced circulating 17β-estradiol levels. 17β-estradiol replacement in SERT−/− mice reversed the obesity and glucose intolerance, supporting a role for estrogen in SERT deficiency-associated obesity and glucose intolerance....." ".... Treatment of wild type mice with paroxetine (SSRI), a chemical inhibitor of SERT, also resulted in Cyp19a1 (aromatase) suppression..."

So, somehow, being SERT-deficient makes you fat and insulin resistant, but also suppresses aromatase and by extension lowers your estrogen levels, the side-effects of which can then be helped by estrogen replacement (?) Fiddling with aromatase -> estradiol in this way seems to mess with fat oxidation and storage. If true, this makes SSRIs even weirder.

From the study;


They reference some interesting studies;
Aromatase-deficient (ArKO) mice have a phenotype of increased adiposity
Chronic Paroxetine Treatment in Mice Leads to Adiposity and Glucose Intolerance

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